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Microbial tryptophan metabolism orchestrated by trilobatin through TPH1 activation protects against acute kidney injury

ABSTRACT: Background: Acute kidney injury (AKI) remains a major clinical challenge with limited therapeutic options. Gut microbiota dysbiosis plays a crucial role in the pathogenesis of AKI. Trilobatin (TLB), has been previously reported to modulate gut microbiota and exert neuroprotective effects; however, its potential role in renal protection remains unknown. Results: In this study, we demonstrate that TLB treatment significantly alleviates renal dysfunction and pathological damage in an AKI mouse model. Moreover, TLB restored intestinal barrier integrity by upregulating key tight junction proteins. 16S rRNA sequencing revealed that TLB modulated the gut microbiota composition, notably enriching Lachnospiraceae, which facilitated tryptophan metabolism and elevated serotonin production. Mechanistically, tryptophan hydroxylase 1 (TPH1) was identified as a direct target of TLB. Conclusions: Our findings unveil a previously unrecognized role of TLB in ameliorating AKI through microbiota-gut-kidney axis regulation, highlighting the therapeutic potential of microbial and metabolic intervention in AKI

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14222 | MetaboLights | 2026-04-05

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14222_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14222_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14222_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS14222_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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